FRANCIANE MOURADIAN EMIDIO TEIXEIRA
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina
LIM/56 - Laboratório de Investigação em Dermatologia e Imunodeficiências, Hospital das Clínicas, Faculdade de Medicina
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- Severe COVID-19 patients show a dysregulation of the NLRP3 inflammasome in circulating neutrophils(2023) LEAL, Vinicius N. C.; ANDRADE, Milena M. S.; TEIXEIRA, Franciane M. E.; CAMBUI, Raylane A. G.; ROA, Mariela E. G. V.; MARRA, Leticia G.; YAMADA, Suemy M.; ALBERCA, Ricardo W.; GOZZI-SILVA, Sarah C.; YENDO, Tatiana M.; NETTO, Lucas C.; DUARTE, Alberto J. S.; SATO, Maria N.; PONTILLO, AlessandraSARS-CoV-2 triggers inflammasome-dependent release of pro-inflammatory cytokine IL-1 beta and pyroptosis, therefore, contributes to the huge inflammatory response observed in severe COVID-19 patients. Less is known about the engagement of inflammasome in neutrophils, main players in tissue injury and severe infection. We studied the activation of the inflammasome in neutrophils from severe COVID-19 patients and assessed its consequence in term of cells contribution to disease pathogenesis. We demonstrated that NLRP3 inflammasome is dramatically activated in neutrophils from severe COVID-19 patients and that the specific inhibition of NLRP3 reverts neutrophils' activation. Next, the stimulation of severe patients' neutrophils with common NLRP3 stimuli was not able to further activate the inflammasome, possibly due to exhaustion or increased percentage of circulating immature neutrophils. Collectively, our results demonstrate that the NLRP3 inflammasome is hyperactivated in severe COVID-19 neutrophils and its exhaustion may be responsible for the increased susceptibility to subsequent (and possibly lethal) infections. Our findings thus include a novel piece in the complex puzzle of COVID-19 pathogenesis.
- A common variant close to the ""tripwire"" linker region of NLRP1 contributes to severe COVID-19(2023) LEAL, Vinicius N. C.; PAULINO, Leandro M.; CAMBUI, Raylane A. G.; ZUPELLI, Thiago G.; YAMADA, Suemy M.; OLIVEIRA, Leonardo A. T.; DUTRA, Valeria de F.; BUB, Carolina B.; SAKASHITA, Araci M.; YOKOYAMA, Ana Paula H.; KUTNER, Jose M.; VIEIRA, Camila A.; SANTIAGO, Wellyngton M. de S.; ANDRADE, Milena M. S.; TEIXEIRA, Franciane M. E.; ALBERCA, Ricardo W.; GOZZI-SILVA, Sarah C.; YENDO, Tatiana M.; NETTO, Lucas C.; DUARTE, Alberto J. S.; SATO, Maria N.; VENTURINI, James; PONTILLO, AlessandraObjective and design The heterogeneity of response to SARS-CoV-2 infection is directly linked to the individual genetic background. Genetic variants of inflammasome-related genes have been pointed as risk factors for several inflammatory sterile and infectious disease. In the group of inflammasome receptors, NLRP1 stands out as a good novel candidate as severity factor for COVID-19 disease. Methods To address this question, we performed an association study of NLRP1, DPP9, CARD8, IL1B, and IL18 single nucleotide variants (SNVs) in a cohort of 945 COVID-19 patients. Results The NLRP1 p.Leu155His in the linker region, target of viral protease, was significantly associated to COVID-19 severity, which could contribute to the excessive cytokine release reported in severe cases. Conclusion Inflammasome genetic background contributes to individual response to SARS-CoV-2.
- Imbalanced IL-1B and IL-18 Expression in Sezary Syndrome(2023) MANFRERE, Kelly Cristina Gomes; TORREALBA, Marina Passos; FERREIRA, Frederico Moraes; SOUSA, Emanuella Sarmento Alho de; MIYASHIRO, Denis; TEIXEIRA, Franciane Mouradian Emidio; CUSTODIO, Ricardo Wesley Alberca; NAKAYA, Helder I.; RAMOS, Yasmin Alefe Leuzzi; SOTTO, Mirian Nacagami; WOETMANN, Anders; ODUM, Niels; DUARTE, Alberto Jose da Silva; SANCHES, Jose Antonio; SATO, Maria NotomiSezary syndrome (SS) is a rare and aggressive type of cutaneous T-cell lymphoma, with an abnormal inflammatory response in affected skin. The cytokines IL-1B and IL-18, as key signaling molecules in the immune system, are produced in an inactive form and cleave to the active form by inflammasomes. In this study, we assessed the skin, serum, peripheral mononuclear blood cell (PBMC) and lymph-node samples of SS patients and control groups (healthy donors (HDs) and idiopathic erythroderma (IE) nodes) to investigate the inflammatory markers IL-1B and IL-18 at the protein and transcript expression levels, as potential markers of inflammasome activation. Our findings showed increased IL-1B and decreased IL-18 protein expression in the epidermis of SS patients; however, in the dermis layer, we detected increased IL-18 protein expression. In the lymph nodes of SS patients at advanced stages of the disease (N2/N3), we also detected an enhancement of IL-18 and a downregulation of IL-1B at the protein level. Moreover, the transcriptomic analysis of the SS and IE nodes confirmed the decreased expression of IL1B and NLRP3, whereas the pathway analysis indicated a further downregulation of IL1B-associated genes. Overall, the present findings showed compartmentalized expressions of IL-1B and IL-18 and provided the first evidence of their imbalance in patients with Sezary syndrome.